According to The National Heart, Lung and Blood Institute (NHLBI) there are approximately 5 million Americans living with congestive heart failure (CHF) and the prevalence of liver cirrhosis is estimated at 400,000 individuals. Both diseases are associated with significant morbidity and mortality. Abnormalities in lymphatic production and drainage are responsible for many symptoms in these diseases. In CHF, increased central venous pressure can lead to decreased lymphatic drainage and increased lymphatic production, which results in CHF symptoms such as tissue edema and liver enlargement. In patients with liver cirrhosis, increased pressure in the hepatic sinusoid can lead to significant increases in liver lymphatic production. When production overcomes the capacity of the system to drain, symptoms can appear in the form of ascites.
Most of the lymphatic fluid that originates in the tissue drains into the thoracic duct (TD), which is the biggest lymphatic vessel in the body. It has been shown that the TD can be significantly distended in patients with liver cirrhosis and CHF. The cause of TD distension is likely due to an increased production of the lymph and elevated TD pressure (1). It has been shown that in patients with CHF, external decompression of the TD can improve symptoms of CHF, such as dyspnea, orthopnea, anorexia, abdominal discomfort, distended neck veins, hepatomegaly, peripheral and scrotal edema and ascites (2, 3). Decompression of the TD has also been shown to resolve ascites in patients with liver cirrhosis (4). External drainage of the TD is invasive and can lead to significant metabolic, immunologic and fluid imbalances. Internal drainage of the TD can overcome these limitations and has been demonstrated to work in both animals and humans. For example, TD to subclavian vein anastomosis to resolve cirrhotic ascites has been described (5, 6). TD to pulmonary vein (PV) shunt has also been described but can require a complicated surgical procedure and its long-teen efficacy is unknown (7). One of the problems with passive decompression of the TD into the venous system is that in most patients with congestive heart failure the pressure in the central venous system is elevated and this increase in pressure has been shown to impede the flow from the TD into the venous system.
Therefore, there remains a need in the art for methods and devices for long-term decompression of the lymphatic system and to alleviate the symptoms associated with CHF and liver cirrhosis.